Aquaporin-1 (AQP1), the archetypal water channel protein, is abundantly expressed in a variety of tissues, including kidney, lung, eye, choroid plexus, and red blood cells. Deficiency of AQP1 was expected to produce a lethal or severe phenotype. Three humas identified with AQP1 deficiency (of six kindreds worldwide) are apparently normal. Recently, APQ1 null mice were found to be normal at baseline, but demonstrated profound defects in urine concentrating ability when water-deprived. These observations lend credence to speculation that human AQP1 "knockouts" are able to compensate for AQP1 deficiency in the unstressed state, but may manifest water transport defects when appropriately stressed. This study will assess that possibility.